There is ample neuropathololgic evidence to suggest that inflammation plays an important role in the progression, and possibly initiation of the disease processes that ultimately lead to Alzheimer?s disease (AD). However little is known about the inflammatory profile of cases compared to non-cases, and whether cases have a predisposition toward a more pro-inflammatory phenotype. The purpose of this PSC is to recruit a sample of AD cases and controls, collect from them biospecimens, and obtain a medical history that can be used to investigate whether AD cases have a different inflammatory profile than controls. Celluar markers of the adaptive immune response The primary function of Th1 T helper cells is to assist the generation of cell-mediated immunity. They secrete a set of cytokines that are generally considered proinflammatory, exemplified by Interferon-? (IFN-?) and IL-12. Th2 cells function to assist humoral immunity, i.e., the generation of immunoglobulin by B cells. Th2 cells secrete a set of cytokines considered at least in some contexts, as anti-inflammatory, such as IL-4 and IL-10. Many of these cytokines have been identified in the neuropathologic material harvested from the brains of AD cases (McGeer and McGeer, 2001). Epidemiologic studies also suggest raised levels of pro-inflammatory cytokines may increase the risk for AD (Schmidt et al., 2002). A recent study demonstrated a Th1-dominated immune response in cases of AD (Remarque et al., 2001). Further, the promising vaccines have been developed on the basis of a humoral immune response to amyloid-a, the putative toxic protein in AD (Schenk et al., 1999).